| Project/Area Number |
11670306
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Virology
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| Research Institution | National Institute of Infectious Diseases (2000)
Kanazawa Medical University (1999) |
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Principal Investigator |
ODAGIRI Takato National Institute of Infectious Diseases, Head, ウイルス第1部, 室長 (80177237)
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| Co-Investigator(Kenkyū-buntansha) |
OHARA Yoshiro Kawazawa Medical University, Professor, 医学部, 教授 (50203914)
小渕 正次 金沢医科大学, 医学部, 助手 (70257450)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | influenza B virus / vRNP complex / BM2 protein / vRNP transport / vRNPの細胞内輸送 / インフルエンザウイルス / ウイルス粒子形成 / two-hybrid |
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| Research Abstract |
The influenza B virus genome RNA segment 7 encodes the M1 and the BM2 proteins. The BM2 protein is synthesized in a coupled translational termination-reinitiation mechanism at the overlapping stop-start penta-nucleotide in a bicistronic messenger RNA transcribed from RNA segment 7. However, features and functions of this protein remain unclear. We characterized the BM2 protein by using an antiserum raised to the BM2 protein of influenza B/Yamagata/1/73 strain. In cells infected with B/Yamagata virus the αBM2 antibody specifically detected the BM2 protein with M_r- 12 k and a polypeptide with M_r- 17 k. When infected cells were labeled with ^<32>Pi and immunoprecipitated with the αBM2 antibody, the ^<32>P-labeled 17 kD polypeptide was specifically precipitated. In the presence of casein kinase inhibitor, CKI-7, the synthesis of the 17 kD and the BM2 proteins was completely suppressed, although other viral proteins except for the polymerase protein were normally synthesized. These results suggested that the 17 kD species was a phosphorylated form of the BM2 protein. These species were substantially synthesized in the late phase of infection and localized in the cytoplasm throughout infection. Moreover, they were transported to the plasma membrane site and thereafter incorporated into virions. These results therefore suggest that the BM2 and the 17 kd proteins should be the components necessary for the life cycle of influenza B virus.
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